HPV E6/E7, O-GlcNAcylation and mitochondrial remodeling in cervical cancer: mechanistic links and translational opportunities
Abstract
Persistent high-risk human papillomavirus (HPV) infection initiates cervical carcinogenesis, while progression and treatment resistance also involve metabolic adaptation. O-GlcNAcylation is a reversible post-translational modification (PTM) controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), with UDP-GlcNAc generated by the hexosamine biosynthetic pathway (HBP) serving as the donor substrate. This review evaluates evidence linking HPV E6/E7-associated metabolic demand, HBP flux, O-GlcNAcylation, and mitochondrial function. We distinguish observations made under untreated conditions from acute treatment responses, identify whether validated resistant models were used, and examine HPV genotype as a source of heterogeneity. Cervical cancer studies support links between O-GlcNAcylation and pathways involved in growth and survival, but no mitochondrial O-GlcNAcylation site has been causally validated in HPV-positive cervical cancer. We therefore grade evidence by model, temporal context, and causal depth and place the proposed relationships within a broader PTM network. This synthesis separates findings obtained in cervical cancer from mechanisms inferred from other systems and identifies the main gaps limiting biomarker and therapeutic development.
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BibTeX
@article{zhang2026e6e7,
title = {{HPV E6/E7, O-GlcNAcylation and mitochondrial remodeling in cervical cancer: mechanistic links and translational opportunities}},
author = {Yingying Zhang and YiMei Tao and Huirong He and Ping Li and Minbin Chen},
journal = {Frontiers in Molecular Biosciences},
year = {2026},
month = oct,
doi = {10.3389/fmolb.2026.1919738},
url = {https://www.frontiersin.org/articles/10.3389/fmolb.2026.1919738},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - HPV E6/E7, O-GlcNAcylation and mitochondrial remodeling in cervical cancer: mechanistic links and translational opportunities
AU - Yingying Zhang
AU - YiMei Tao
AU - Huirong He
AU - Ping Li
AU - Minbin Chen
PY - 2026
DA - 2026/10/30
JO - Frontiers in Molecular Biosciences
DO - 10.3389/fmolb.2026.1919738
UR - https://www.frontiersin.org/articles/10.3389/fmolb.2026.1919738
AB - Persistent high-risk human papillomavirus (HPV) infection initiates cervical carcinogenesis, while progression and treatment resistance also involve metabolic adaptation. O-GlcNAcylation is a reversible post-translational modification (PTM) controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), with UDP-GlcNAc generated by the hexosamine biosynthetic pathway (HBP) serving as the donor substrate. This review evaluates evidence linking HPV E6/E7-associated metabolic demand, HBP flux, O-GlcNAcylation, and mitochondrial function. We distinguish observations made under untreated conditions from acute treatment responses, identify whether validated resistant models were used, and examine HPV genotype as a source of heterogeneity. Cervical cancer studies support links between O-GlcNAcylation and pathways involved in growth and survival, but no mitochondrial O-GlcNAcylation site has been causally validated in HPV-positive cervical cancer. We therefore grade evidence by model, temporal context, and causal depth and place the proposed relationships within a broader PTM network. This synthesis separates findings obtained in cervical cancer from mechanisms inferred from other systems and identifies the main gaps limiting biomarker and therapeutic development.
SN - 2296-889X
ER -